Jung Da-hyun is a reporter at The Korea Times, covering social issues in Korea, including foreign residents, education, environment and politics. Driven by a deep interest in people’s stories, she focuses on investigative and feature reporting through direct interviews and field coverage. She received the Amnesty International Korea Media Award for her “Deepfake Crisis at Schools” series. Reach her at dahyun08@koreatimes.co.kr. Always open to hearing your stories.
Yonsei Univ. team pioneers new method to target cancer metabolism
Park Hyun-woo, left, a biochemistry professor at Yonsei University, and Peon Woo-yang, a researcher in Park’s team / Courtesy of Yonsei University
By Jung Da-hyun
A research team led by Park Hyun-woo, a biochemistry professor at Yonsei University, has introduced a pioneering method in Oncometabolic Precision Medicine — a breakthrough approach that aims to treat cancer by targeting the unique way tumors metabolize nutrients.
The team demonstrated that a cancer patient’s nutritional and metabolic status is a decisive factor in determining the efficacy of anticancer therapies, offering a new treatment framework based on customizing care to exploit these metabolic vulnerabilities.
The study found that the sensitivity of cancer cells to drugs varies significantly depending on each patient’s blood metabolite levels, offering new possibilities for personalized anticancer treatment guidelines based on metabolic profiling.
The results were published in the latest issue of Cancer Research, the flagship journal of the American Association for Cancer Research.
Park’s team built a Cancer Metabolism–based Synthetic Lethality Platform by testing 1,813 U.S. FDA-approved non-oncology drugs while altering concentrations of metabolites typical of the tumor microenvironment — such as glucose, glutamine and fatty acids — and measuring cancer cell viability.
Through this platform, the researchers discovered new molecular mechanisms by which existing cardiovascular anti-arrhythmia drugs, diabetes medications and other non-oncology treatments can maximize cancer cell death depending on metabolic conditions.
In particular, the anti-arrhythmic drug propafenone induced cancer-specific cell death only under low-glucose conditions, triggering AMPK–mTOR pathway suppression within cancer cells. Meanwhile, the type-2 diabetes medication, metformin, inhibited Hippo–YAP signaling, demonstrating anticancer activity across multiple tumor types. By contrast, the veterinary anthelmintic fenbendazole showed its strongest anticancer effects exclusively under high-glucose conditions.
These findings show that cancer cells experience different metabolic stress responses depending on a patient’s metabolic status. Clinically applying such differences could yield a new personalized treatment strategy that boosts anticancer effectiveness while reducing side effects.
“This study provides systematic evidence that drug responsiveness can be predicted from a patient’s nutritional metabolic map — their blood glucose, fatty acid and amino acid levels,” Park said. “It goes beyond precision medicine that focuses only on genetic mutations and signals a shift toward a new era of cancer metabolism–based precision medicine that incorporates metabolic profiles.”